Cases reported "Wernicke Encephalopathy"

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1/28. Downbeat nystagmus caused by thiamine deficiency: an unusual presentation of CNS localization of large cell anaplastic CD 30-positive non-Hodgkin's lymphoma.

    A 24-year-old woman with a large cell anaplastic CD 30-positive T-cell non-Hodgkin's lymphoma (NHL) developed downbeat nystagmus, anisocoria, and oscillopsia. Prior to overt cerebral invasion by NHL, she had a thiamine deficiency with very low thiamine concentrations in the CSF, probably caused by protracted vomiting and increased vitamin B1 consumption by intrathecal tumor cells. We believe that her neurologic symptoms were caused -- at least partly -- by thiamine deficiency, as she reacted well to thiamine supplementation at the beginning of treatment.
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2/28. Wernicke's encephalopathy induced by hyperemesis gravidarum.

    A report is presented on a patient with Wernicke's encephalopathy secondary to hyperemesis gravidarum. The 25-year-old female presented 11 weeks into pregnancy with prolonged vomiting. Neurological examination 8 weeks later demonstrated obtunded sensations, nystagmus and ataxia of gait. MR imaging revealed bilateral lesions in the mediodorsal nuclei of thalami, in the hypothalamus and in the periaqueductal gray matter (1). The neurological signs and the MRI findings pointed to a diagnosis of Wernicke's encephalopathy. The patient was treated with intramuscular vitamin B1 followed by oral thiamine until the end of pregnancy. The subsequent course of the pregnancy was uncomplicated, and resulted in the delivery of a healthy 2970 g male infant. A review of the literature published during the last 30 years revealed an additional 20 cases of Wernicke's encephalopathy induced by hyperemesis gravidarum. Only half of these pregnancies resulted in the birth of a normal infant.
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3/28. Gestational thyrotoxicosis with acute wernicke encephalopathy: a case report.

    A 35-year-old hyperthyroid woman who developed nausea, vomiting, tachycardia, nystagmus and mental disturbance, was referred to our hospital with a suspected diagnosis of thyroid storm. However, the thyroid gland was only slightly palpable, bruits were not audible, and exophthalmos was not present. serum levels of thyroid hormone were increased, but TSH receptor antibodies were negative. Echography and color flow doppler ultrasonography revealed a slightly enlarged thyroid gland and a slightly increased blood flow, both of which were much less milder than those expected for severe hyperthyroid Graves' disease. Under the diagnosis of hyperthyroidism due to gestational thyrotoxicosis associated with wernicke encephalopathy, vitamin B1 was administered on the first day of admission. Her consciousness became nearly normal on the second day except for slight amnesia. Her right abducent nerve palsy rapidly improved, but horizontal and vertical nystagmus, diminished deep tendon reflexes and gait ataxia improved only gradually. MRI findings of the brain were compatible with acute wernicke encephalopathy. We concluded that history taking and physical findings are important to make a differential diagnosis of gestational thyrotoxicosis with acute wernicke encephalopathy from Graves' thyroid storm, and that wernicke encephalopathy should be treated as soon as possible to improve the prognosis.
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4/28. Wernicke's encephalopathy following gastroplasty for morbid obesity.

    BACKGROUND: The syndrome of Wernicke's encephalopathy consists of two of four features of (1) dietary deficiency; (2) oculomotor abnormality; (3) cerebellar dysfunction; and (4) confusion or mild memory impairment. Predisposing risk factors include alcoholism, hyperemesis gravidarum and prolonged intravenous feeding. methods: A 35-year-old female developed refractory emesis, severe weight loss, and hypokalemia following banded gastroplasty for morbid obesity. Reversal of gastroplasty was performed four months following initial surgery. Following reversal, the patient developed confusion, ataxia, leg weakness and nystagmus. RESULTS: Examination of the patient demonstrated disorientation with confusion, vertical nystagmus worse on downgaze, diffuse weakness of the lower extremities, and bilateral dysmetria. magnetic resonance imaging of the brain demonstrated symmetrical areas of increased T2 signal present bilaterally in the medial thalamic nuclei. The patient did not demonstrate any initial improvement with intravenous thiamine but improved over two months of follow-up. CONCLUSION: Wernicke's encephalopathy has been reported in the European literature as a complication of gastroplasty, with rare recognition of this clinical entity in the North American literature. This potential complication of gastroplasty may be preventable by nutritional intervention in subjects experiencing severe weight loss and emesis following surgery.
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5/28. Wernicke's encephalopathy due to hyperemesis gravidarum: an under-recognised condition.

    We present a case of a 25-year-old woman with drowsiness, nystagmus, severe ataxia and areflexia, which developed six weeks after admission to an obstetric clinic for hyperemesis gravidarum. She had been treated with intravenous dextrose and electrolyte solutions and antiemetics. magnetic resonance imaging (MRI) performed on the fifth day of her neurologic symptoms showed increased intensity in both thalami, periaqueductal grey matter, the floor of the fourth ventricle and superior cerebellar vermis in T2 weighted and FLAIR images. Clinical signs and MRI findings were consistent with the diagnosis of Wernicke's encephalopathy. On the third day of thiamine replacement, neurologic signs improved dramatically In addition to our case, we review 29 previously reported cases of Wernicke's encephalopathy associated with hyperemesis gravidarum, and emphasize the importance of thiamine supplementation to women with prolonged vomiting in pregnancy especially if they are given intravenous or parenteral nutrition.
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6/28. Wernicke's encephalopathy presenting with upbeating nystagmus.

    The case of a 49-year-old woman with Wernicke's encephalopathy is described, in which primary position upbeating nystagmus was the chief ocular sign. Although there was no history of excessive alcohol consumption, Wernicke's encephalopathy was diagnosed on a background of anorexia nervosa. The diagnosis was supported by the patient's symptomatic and clinical recovery following thiamine therapy.
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7/28. Caloric-eye tracking pattern test: I. Visual suppression and the possibility of simplified differential diagnosis between peripheral and central vertigo.

    During the examination of patients who complain of vertigo or who have equilibrium disorders, it is often difficult to determine the etiology of the disorders, that is, to determine whether it is dependent on a peripheral or central vestibular disorder. To attempt to guess the etiology in these cases, we devised a new method: the caloric eye-tracking pattern test. In normal subjects and in patients with peripheral disorders, as is well known, caloric nystagmus has little influence on the eye-tracking pattern. In contrast, in patients with central vestibular disorders, caloric nystagmus evoked abnormalities on the eye-tracking pattern, either superimposed or saccades, in spite of the fact that the eye-tracking pattern before the caloric stimulation is normal. These findings result from the visual suppression mechanism to the vestibular nystagmus. We can say that the visual suppression to the vestibular nystagmus is evoked more strongly bu pursuing a moving visual stimulus than by gazing at a stationary target. These results are interesting, not only form the physiological view point, but also from the clinical view point. There is a possibility of the differential diagnosis between peripheral and central vertigo.
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8/28. Presumed pharmacologically induced change from upbeat- to downbeat nystagmus in a patient with Wernicke's encephalopathy.

    A case of Wernicke's encephalopathy due to proven thiamine deficiency suffering from upbeat nystagmus (UN) changing to downbeat nystagmus (DN) after a latency of 1 year is presented. The case was also notable for the finding of positive oligoclonal bands in the CSF. The underlying pathophysiological mechanisms and a possible effect of baclofen treatment are discussed.
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9/28. Transition from upbeat to downbeat nystagmus observed in a patient with Wernicke's encephalopathy.

    BACKGROUND: We report an unusual case of Wernicke's encephalopathy presenting with transient upbeat nystagmus that changed to a persistent downbeat nystagmus. CASE: A 27-year-old man presented with upbeat nystagmus. Three months earlier, he had been diagnosed with Wernicke's encephalopathy after fasting for a month. OBSERVATIONS: This diagnosis was supported by his symptoms (ataxia, a confused state). Clinical recovery followed thiamine therapy. His upbeat nystagmus had linear slow phases with average amplitude and frequency ( /-SD) during fixation straight ahead of 2.8 /- 0.7 degrees and 4.6 /- 2.2 Hz, respectively. Two months later, the primary position upbeat nystagmus had diminished and downbeat nystagmus (0.9 /- 0.5 degrees and 3.2 /- 0.7 Hz on average) for a 20 degrees downward gaze had developed. Then, 8 months later, he showed only downbeat nystagmus, which obeyed Alexander's law. His primary position downbeat nystagmus was completely suppressed by clonazepam, a gamma-aminobutyric acid (GABA) agonist. CONCLUSIONS: Owing to an underlying central vestibular imbalance, even after the recovery of acute neurological symptoms, Wernicke's encephalopathy can be complicated by persistent downbeat nystagmus, which can be treated by a GABA agonist.
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10/28. Acute ophthalmoplegia and nystagmus in infants fed a thiamine-deficient formula: an epidemic of wernicke encephalopathy.

    In 2003, an epidemic of wernicke encephalopathy (WE) developed in Israeli infants fed a thiamine-deficient soy-based formula. Approximately 20 infants were affected out of an estimated 3500 fed the vitamin-deficient formula. The finding of gaze abnormalities in a single infant by neuro-ophthalmologists led to the unraveling of the epidemic. In this report, the findings in three infants are described. early diagnosis and treatment with parenteral thiamine led to complete neurologic recovery in two infants; in the third infant, delayed diagnosis may have been responsible for severe lingering deficits. This is the first reported epidemic of WE secondary to thiamine-deficient infant formula. early diagnosis and treatment are critical to avoid persistent neurologic impairment.
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